Non-carious lesions of teeth that appears before teeth eruption. Classification, pathomorphology, clinic, diagnosis, differential diagnosis and treatment of un-carious lesions.


Classification of non-carious lesions:

I. Lesions that occur in the stage of dental follicle development, before eruption:

1. hypoplasia;

2. hyperplasia of enamel (enamel pearls);

3. endemic fluorosis;

4. developmental disturbances and disorders of eruption;

5. genetic disturbances of tooth development.

II. Lesions that occur after teeth have been erupted:

1. tooth wear: attrition, abrasion, wedge-shaped defect;

2. erosion;

3. necrosis of hard tooth tissues;

4. hyperesthesia;

5. trauma of teeth;

6. fluorosis;



Disturbed Tooth Eruption

Tooth eruption comprises the movement of teeth through the soft tissues of the jaw and the overlying mucosa into the oral cavity involved biological processes are not yet entirely elucidated, but the importance of the dental follicle has been established beyond doubt. Teeth may erupt too early, too late, not in the proper position, or not at all. In the latter event, one speaks of impaction. It is most often seen in lower 3rd molar teeth.

Premature Eruption

Both deciduous as well as permanent teeth may erupt into the oral cavity at a too-early age. Because the roots are not yet well developed at that time, the fixation of the tooth in the jaw may be compromised and the subsequent root development may be disturbed, resulting in teeth with malformed and/or too-short roots.

Sometimes, the teeth exfoliate spontaneously due to lack of a well-formed root and periodontal ligament. Premature eruption may occur as one of the abnormalities of the Hallermann-Streift syndrome.


Developmental tooth anomalies

Developmental disturbances of the teeth may be inherited or they may be acquired and the result of environmental disturbances. In all cases the disturbances occur during the period of tooth formation which may be either before and/or after birth. Developmental disturbances which occur early in tooth development affect the shape (form) of teeth, their number or size. Those which occur later during the formation of the dental hard tissues result in disturbances of tooth structure.

Disturbances in the number of teeth


Hypodontia is a decrease in the number of teeth compared with normal and is relatively common in the permanent dentition (although rare in the primary dentition). The most common missing teeth are:

■ Lower third molars.

■ Upper lateral incisors.

■ Lower second premolars.

In some cases there is a hereditary trait but many cases appear sporadically.

Fig. Congenital absence of lateral incisors with spacing of the

anterior teeth.



Anodontia is a total absence of teeth and is very unusual. It usually occurs in association with a hereditary genetic condition, hypohidrotic ectodermal dysplasia. The condition is caused by a gene defect in which patients have very few or no teeth, and absence of hair and sweat glands.

Supernumerary teeth

An additional tooth in the arch is known as a supernumerary tooth. They are more common in the permanent than the primary dentition and affect females more than males. Supernumerary teeth may occur at any site but are more common in the anterior maxilla and the premolar region of the mandible. Different types of supernumerary teeth are recognised. These are:

■ Mesiodens a supernumerary tooth that develops between the upper central incisors. This is the most common type of supernumerary tooth.

■ Paramolar an additional molar tooth.

■ Supplemental teeth additional teeth that resemble normal teeth.

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Fig. Two mesiodens: supernumerary teeth in the midline

between the upper central incisors. Note the marked crowding.


Clinical importance

Supernumerary teeth may prevent the eruption of a permanent tooth and should always be considered if a tooth fails to erupt. Similarly, a supernumerary tooth may cause displacement or malposition of teeth and, if unerupted, may resorb teeth.

Disturbances of tooth size

Tooth size is determined by genetic factors and abnormally large or small teeth may occur. Usually the entire dentition is affected but sometimes only a few teeth may be excessively large or small. Small teeth may occur in association with missing teeth; for example, one missing upper lateral incisor may be associated with a small peg-shaped lateral incisor on the other side.

Fig. Hypodontia before and after treatment.



Enamel pearls

Enamel pearls are uncommon, minor abnormalities, which are formed on otherwise normal teeth by displaced ameloblasts below the amelocemental junction. Enamel pearls may consist of only a nodule of enamel attached to the dentine, or may have a core of dentine containing a horn of the pulp. The pearls are usually round, a few millimetres in diameter, and often form at the bifurcation of upper permanent molars. They may cause a stagnation area at the gingival margin, but, if they contain pulp, this will be exposed when the pearl is removed.


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Fig. Enamel pearl. There is a small mass of enamel at the root




Disturbances in the structure of teeth

Disturbances in the structure of teeth may affect the enamel or dentine or sometimes both. Those which affect the enamel are more obvious clinically.

Disturbances of enamel

Developmental disturbances of enamel are relatively common and are usually the result of a localised or generalised environmental disturbance occurring during tooth development. Only a few are the result of a genetic defect. The causes are summarised below:

■ Genetic disturbances

- Amelogenesis imperfecta.

■ Local disturbances:

- Infection.

- Trauma.

- Idiopathic.

■ Generalised disturbances:

- Infections.

- Fluorosis.

- Neonatal events, e.g. premature birth, rhesus incompatibility.

Amelogenesis imperfecta

This is the name given to a group of inherited disorders which result in defective enamel formation. Most are the result of defects in genes which code for either enamel matrix production or the mineralisation of enamel.

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Fig. Amelogenesis imperfecta of the hypoplastic type. Tooth surface shows pitting

(a) or irregularities (b) indicating abnormal enamel formation. The hardness of the enamel is normal


The clinical features are variable and depend on which gene is defective:

■ In some forms the teeth appear normal on eruption but, because the enamel is poorly mineralised, it is soft and soon wears away. The remaining enamel becomes stained and the teeth appear yellowbrown.

■ In other forms the enamel is reduced in amount and the teeth are pitted and appear yellowbrown in colour.

■ Some forms are carried on the X chromosome and boys are affected more severely than girls.

■ The teeth are often sensitive, especially where the enamel is thin or has chipped away.

Hypomaturation amelogenesis imperfecta

The enamel is normal in form on eruption but opaque, white to brownish-yellow. The teeth appear similar to mottled fluoride effects. However, they are soft and vulnerable to attrition, though not as severely as the hypocalcified type. There are several variants of hypomaturation defects such as a more severe, autosomal dominant (type 4) of hypomaturation combined with hypoplasia.


Fig. Amelogenesis imperfecta, hypomaturation type. Tooth

morphology is normal but there are opaque white and discoloured



Hypocalcified amelogenesis imperfecta

Enamel matrix is formed in normal quantity but poorly calcified. When newly erupted, the enamel is normal in thickness and form, but weak and opaque or chalky in appearance. The teeth tend to become stained and relatively rapidly worn away. The upper incisors may acquire a shouldered form due to the chipping away of the thin, soft enamel of the incisal edge. There are dominant and recessive patterns of inheritance.


Fig. Amelogenesis imperfecta, hypocalcified type. The soft chalky

enamel was virtually of normal thickness and form but has chipped away

during mastication.


Acquired disturbances of enamel formation

Most acquired enamel defects result in areas of hypoplasia, which may be due to either a defect in matrix production or a defect in mineralisation. If only a single tooth is affected these are classified as localized disturbances, but if several teeth are affected then they are referred to as generalized.

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Fig. White spot on labial surface of right first incisor

tooth indicates transient period of hypocalcification

Localised defects most commonly affect the upper incisor teeth or premolars and usually form as a result of infection (follicles of premolars are placed between roots of temporary molars that are very often have apical periodontitis) or trauma to the deciduous predecessor. This affects the ameloblasts of the developing tooth, resulting in the production of enamel which may be yellowbrown, pitted or irregular. These teeth are sometimes referred to as Turner teeth.

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Fig. Turner tooth. The upper central incisor is markedly hypoplastic and brown in color.


Enamel opacities are opaque white spots sometimes seen particularly on the upper central incisors. They may become stained with time. The cause of these opacities is not known but they are relatively common.

Generalised defects are sometimes referred to as chronological hypoplasias and most are the result of a generalised or systemic infection or disturbance occurring during tooth development. The disturbance affects enamel formation and results in a linear horizontal band of hypoplasia. This may be characterised by ridging or grooving or pitting on the enamel surface and the teeth that are affected are those which were forming at the time of the disturbance. Thus with a knowledge of the times of crown formation it is possible to predict at what age a patient was systemically unwell. The overwhelming majority of chronological hypoplasia as are the result of disturbances in the first 10 months of life and the teeth affected are:

■ The first permanent molars.

■ Upper central incisors.

■ Lower lateral incisors and canines.

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Fig. Chronological hypoplasia due to metabolic upset. Unlike the

hereditary types of amelogenesis imperfecta, defects are linear and

thought to correspond to a short period of amelogenesis disturbed by a

concurrent severe illness.


However, disturbances may occur before birth or during the neonatal period. Common causes of disturbances are viral infections, such as measles and mumps, and excess fluoride ions. In the prenatal period, diseases affecting the mother may be important.


Enamel hypoplasia is a defect that occurs when dental enamel doesnt form completely, usually because of malnutrition or disease. Enamel hypoplasia is identified as a horizontal line, a series of pits or grooves along the outer surface of the tooth. These lines mark points at which the bones growth was resumed after it had stopped. The degree of hypoplasia is proportional to the length of time the growth was arrested. Hypoplasia does not form in individuals who are chronically ill or malnourished; it only occurs in healthy individuals.

Hypoplasia is most common in the permanent teeth and represents episodes of arrested growth in infancy or childhood while these teeth were still developing. Once the enamel forms, it can not longer be affected.

Hypoplasia in deciduous or baby teeth is extremely rare since the fetus is usually well nourished in the womb. A case of hypoplasia in the baby teeth is generally a sign that the baby was born prematurely or was nurtured in the womb of a very sick woman.

Hypoplasia in young childrens teeth is usually an indication that the mother was malnourished while pregnant or nursing.

Fig. 1 Enamel hypoplasia.


Conditions preceding EHP


Low birthweight


Maternal illness


Drug abuse

Liver disease

Other systemic diseases


Congenital syphilis

Prenatal syphilis, the result of maternal infection, can cause a characteristic dental deformity, described by Hutchinson in 1858.

If the fetus becomes infected at a very early stage, abortion follows. Infants born with stigmata of congenital syphilis result from later fetal infection, and the permanent teeth are affected. The characteristic defects are usually seen in the upper central incisors.

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Fig. Congenital syphilis; Hutchinson's teeth. The characteristics

are the notched incisal edge and the peg shape tapering from neck to tip.


The incisors (Hutchinson's incisors) are small, barrel-shaped, and taper towards the tip. The incisal edge sometimes shows a crescentic notch or deep fissure which forms before eruption and can be seen radiographically. An anterior open bite is also characteristic. The first molars may be dome-shaped (Moon's molars) or may have a rough pitted occlusal surface with compressed nodules instead of cusps (mulberry molars). These defects are now largely of historical interest.


The effects are due to infection of the dental follicle by Treponema pallidum. The postulated consequences are chronic inflammation, fibrosis of the tooth sac, compression of the developing tooth and distortion of the ameloblast layer. T. pallidum causes proliferation of the odontogenic epithelium which bulges into the dentine papilla causing the characteristic central notch.

Tetracycline Discoloration

Tetracycline is taken up by calcifying tissues, and the band of tetracycline-stained bone or tooth substance fluoresces bright yellow under ultraviolet light. The teeth become stained only when tetracycline is given during their development, and it can cross the placenta to stain the developing teeth of the fetus. More frequently, permanent teeth are stained by tetracycline given during infancy. Tetracycline is deposited along the incremental lines of the dentine and, to lesser extent, of the enamel. The more prolonged the course of treatment the broader the band of stain and the deeper the discolouration. The teeth are at first bright yellow, but become a dirty brown or grey. The stain is permanent, and when the permanent incisors are affected the ugly appearance can only be disguised. When the history is vague the brownish colour of tetracycline-stained teeth must be distinguished from dentinogenesis imperfecta. In dentinogenesis imperfecta the teeth are obviously more translucent than normal and, in many cases, chipping of the enamel from the dentine can be seen. In tetracycline-induced defects the enamel is not abnormally translucent and is firmly attached to dentine. In very severe cases, intact teeth may fluoresce under ultraviolet light. It is no longer necessary to give tetracycline during dental development. There are equally effective alternatives and it should be avoided from approximately the fourth month to 12th year of childhood. Nevertheless tetracycline pigmentation is still seen.

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Fig. Tetracycline staining. Note the chronological distribution of

the dark-brown intrinsic stain.


Trough binding to calcium, tetracyclin is deposited together with calcium in any tissue undergoing mineralisation. After its incorporation during mineralisation, it can be demonstrated in teeth and bones in ultraviolet light, showing up as fluorescent yellow bands. Grossly, tetracyclin causes a greyish-black discoloration of the tooth

crown (Figs. ac).

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Fig. Tetracyclin discoloration:

a)    Outer view showing grey discoloration of crown and yellow discoloration of upper part of the root.

b)    Cut surface showing the band-like appearance of the discoloration indicating several administrations of the drug.

c)     Ground section also illustrating the band-like discolorations in the enamel and a tiny yellow line in the dentin.


When making ground sections of these teeth, the tetracyclin bands can be observed under UV light illumination both in dentin as well as in enamel, each band indicating a time point of tetracyclin administration. After decalcification the tetracyclin has been lost together with the calcium and therefore, in decalcified paraffin sections, this fluorescence is not present anymore.

Treatment of hypoplastic defects

Hypoplastic teeth can be disguised by restorative procedures such as veneers or jacket crowns. The latter should be delayed until adult life. The young pulp is large, is easily damaged during preparation of the tooth, and injuries are more frequent than in older persons.


Disturbances of dentine

Like defects of enamel, the dentine may be affected by acquired and by genetic defects. However, acquired dentinal defects cause very few problems and only genetic defects are of clinical significance.

Dentinogenesis imperfecta

This genetic disorder is characterised by defective dentine matrix production and two types have been described. Dentinogenesis imperfecta type 1 occurs in association with osteogenesis imperfecta, in which there is defective bone formation. It is very uncommon.

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Fig. Dentinogenesis imperfecta. Note the brown color of the dentine and the marked attrition.

Dentinogenesis imperfecta type 2 is the commonest form. It has the following features:

■ Both the permanent and primary dentition are affected.

■ The teeth have a normal shape on eruption but appear amberbrown or purpleblue in colour.

■ The enamel shears away from the poorly formed dentine which quickly wears away.

■ The pulps become obliterated with abnormal dentine.

Patients suffer marked attrition and this can cause severe problems. The aim of treatment is to prevent attrition with the restoration of lost tooth substance and the provision of crowns if necessary.

Developmental Structural Abnormalities Involving Both Enamel and Dentin


Odontodysplasia is a developmental disturbance consisting of both enamel and dentin abnormalities in several adjacent teeth. The often-added suffix regional emphasises this usually localised character, but a few cases have been described with involvement of more extensive parts of the dentition, the abnormal teeth being present bilaterally and in both upper and lower jaw.

Fig. Radiographic appearance of regional odontodysplasia. On one

side of the midline the deciduous incisors have poor root formation with

thin radicular dentine and enamel. A poorly organised spotty calcification

is present at the site of the permanent successors.


The teeth are abnormally formed and the covering enamel layer is thin and yellow. The pulp chambers are wide and the amount of dentin is greatly reduced. The enamel is hypoplastic and the dentin contains large areas of interglobular dentin. Also, the predentin zone is very wide. The dental pulp usually contains large and irregular aggregates of mineralised matrix, the so-called denticles. The condition may be accompanied by gingival enlargement.

Odontogenesis Imperfecta

In odontogenesis imperfecta, both enamel and dentin exhibit pathologic changes in all teeth. The enamel is hypoplastic and the dentin shows changes similar to those seen in dentinogenesis imperfecta.

Shell teeth (dentinogenesis imperfecta)

Fig. Shell tooth. In this severe form of dentinogenesis imperfecta

only a thin mantle of dentine is formed and no root develops


This rare anomaly is so called because only a thin shell of hard dental tissue surrounds overlarge pulp chambers. Like other types of dentinogenesis imperfecta there is normal, but thin, mantle dentine which covers irregular dentine. The pulp lacks a normal odontoblast layer and consists of coarse connective tissue which becomes incorporated into the deep surface of the dentine.



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Fig. Fluorosis. Moderate effects from an area of endemic fluorosis.

Irregular patchy discolouration.


Fluorosis continues to be an endemic problem. The following countries have been identified for the problem of fluorosis: Pakistan, Bangladesh, Argentina, United States of America, Morocco, Middle East countries, Japan, South African Countries, New Zealand, Thailand etc. Children in the age group of 0 to 12 years are most prone to fluorosis as their body tissues are in formative / growth stage during this period. Expectant mothers are also to be protected, as there is growing concern about effects of fluoride on fetus. Acceptable measures of fluorine in water according to hygienic standards is - 0,8-1,2(1,5)mg/l. Fluorosis is the term given to changes in the enamel which are associated with excess ingestion of fluoride. These vary from localised white opacities to more severe brownyellow mottling on the teeth. The precise effect depends on the dose of fluoride (from all sources), the duration for which it was taken and the age of the patient at the time of ingestion. Fluorosis when very severe (concentrations in the water supply greater than six parts per million) may result in extensive hypoplasia with brown staining.

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Fig. Left: Enamel fluorosis of mild to moderate severity is seen across much of this patients dentition.

Right: Mild to moderate enamel fluorosis is more localized in this patient.


Table. Distinctive features of dental fluorosis

Mottling is endemic in areas where fluorides in the drinking water exceed about 2 parts per million, i.e. it has a geographical distribution

Neighbouring communities with fluoride-free water do not suffer from the disorder

Only those who have lived in a high-fluoride area during dental development show mottling. The defect is not acquired by older visitors to the area

Permanent teeth are affected; mottling of deciduous teeth is rare

Mottled teeth are less susceptible to caries than normal teeth from low-fluoride areas

A typical effect is paper-white enamel opacities

Brown staining of these patches may be acquired after eruption

Clinical features

Mottling ranges from paper-white patches to opaque, brown, pitted and brittle enamel. Clinically, it may be difficult to distinguish fluorotic defects from amelogenesis imperfect when the degree of exposure to fluoride is unknown. There is considerable individual variation in the effects of fluorides. A few patients acquire mottling after exposure to relatively low concentrations, while others exposed to higher concentrations appear unaffected. Changes due to mottling are graded as shown in Table.




Table. Grading of mottled enamel

Very mild. Small paper-white areas involve less than 25% of surface

Mild. Opaque areas involve up to 50% of surface

Moderate. The whole of the enamel surface may be affected with

paper-white or brownish areas or both

Severe. The enamel is grossly defective, opaque, pitted, stained

brown and brittle




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Fig. Fluorosis. Severe effects from an area of endemic fluorosis.

Closer view showing irregular depressions caused by hypoplasia and

white opaque flecks and patches.



Fig. Fluorosis. Moderate form


Fig. Mild form of fluorosis

Type and stages of dental fluorosis

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5. Un-carious lesions of teeth that appears after teeth eruption. Pathomorphology, clinic, diagnosis and treatment of un-carious lesions.


Classification of un-carious lesions:

I. Lesions that occur in the stage of dental follicle development, before eruption:

1. hypoplasia;

2. hyperplasia of enamel (enamel pearls);

3. endemic fluorosis;

4. disorders of development and eruption;

5. genetic disturbances of tooth development.

II. Lesions that occur after teeth have been erupted:

1. tooth wear: attrition, abrasion, wedge-shaped defect;

2. erosion;

3. necrosis of hard tooth tissues;

4. hyperesthesia;

5. trauma of teeth;

6. fluorosis;


Tooth wear

Tooth wear is defined as loss of tooth tissue due to causes other than caries. Some tooth wear is normal and occurs with age. This is termed physiological tooth wear. However, excessive tooth wear is pathological. Three types have been described: attrition, abrasion and erosion. Although these may occur separately, in many instances they occur together.


Attrition is the process of wearing away of enamel, which occurs physiologically as a consequence of mastication. This process is very slow and results in a gradual loss of enamel. Pindborg disitinguished three types of attrition: physiological, excessive and pathological. The dental pulp cavity is usually not open due to attrition.


Fig. Attrition.

This patient has marked attrition of the occlusal surfaces of most of his teeth.


Attrition is tooth wear caused by tooth-to-tooth contact. It occurs as a normal part of ageing and it is usually the incisal edges which wear away first, followed by the occlusal surfaces of the molar teeth. There may also be loss of interproximal tooth tissue leading to mesial migration of the teeth. Excessive occlusal wear may occur in the following situations:

■ Patients with bruxism. These patients grind their teeth excessively and in some cases this is triggered by occlusal irregularities.

■ Patients who have lost several posterior teeth may show excessive attrition of the anterior teeth, especially if these are used for chewing.

■ Patients who suffer from developmental disturbances of tooth structure, such as amelogenesis and dentinogenesis imperfecta, may suffer exceptional tooth wear.

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Fig. Attrition: mandibular incisor teeth with enamel worn away thus exposing the brown discolored dentin.



Abrasion is frictional tooth loss caused by extrinsic agents. It is always pathological and may be caused by tooth brushing and habits such as biting on a pipe or a pencil. Tooth brush abrasion is characteristic and is caused by poor tooth brushing technique, i.e. patients brushing horizontally with excessive force. It has the following characteristics:

■ It particularly affects the labial and buccal surfaces of the upper incisor, canine and premolar teeth.

■ The resulting cavity is wedge-shaped with a sharp angle towards the occlusal surface and an obtuse angle towards the apical surface.

■ The problem is often compounded by the use of hard tooth brushes and abrasive tooth paste.

Fig. Erosive-abrasive defect in the upper jaw involving all teeth except for tooth 16.


Abrasion is defined as a defect of hard dental tissues caused by the mechanical action of abrasives on the tooth surface. It is found most frequently in the region of the tooth cervix as a wedge-shaped defect. The loss of both dentin and enamel is present.


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Fig. Wedge-shaped defect

These wedge-shaped defects can lead to the denudation of dental pulp. At the beginning, the smooth walls of the defect are very sensitive to various (mechanical, chemical or physical) stimuli but later this sensitivity descreases. Wedge-shaped defects are usually to be one of the characteristic symptoms of chronic generalized periodontitis.


Erosion is the loss of tooth substance caused by chemical agents and is non-bacterial and therefore does not include loss by caries. Most erosion is caused by acids and is seen in the following groups:

■ Those with gastric reflux and with bulimia and anorexia. Regurgitation of acid from the stomach particularly affects the palatal surfaces of the upper maxillary teeth.

■ As an occupational hazard. Those who work in an acidic environment, e.g. in factories making batteries, and also in wine tasters. Erosion in these groups is relatively rare but because the acid is in the environment the erosion is particularly seen on the labial surfaces of both the upper and lower incisor teeth.

■ Those who consume excessive amounts of carbonated soft drinks or fruit juices. This group is by far the largest and in the Western world it is particularly children, adolescents and young adults who are affected.

The surfaces which are most commonly affected are the palatal surfaces of the upper anterior teeth. The teeth may appear yellow due to the reduction in the thickness of the enamel and typically the cavities are shallow and broad. Patients with erosion may be unaware that they have a problem but others may complain of sensitivity, particularly on eating hot and cold foods.

Fig. Erosion: buccal surfaces of right maxillary cuspid and first premolar tooth showing loss of enamel. Both central and right lateral incisor teeth show white areas at their labial surfaces indicating incipient decalcification but still maintaining their crystalline structure


There is no doubt, the process of tooth wear is often the combination of two or all three factors and those that are more likely to occur are erosion and attrition.

Acids in the mouth cause the surface of the tooth to be weakened which allows tooth-to-tooth contact during mastication to effect greater loss of the tooth surface than would otherwise be the case if erosion or attrition were occurring alone. The source of the acid may be intrinsic, arising from gastric acid escaping from the stomach into the oesophagus and then into the mouth. This may be a result of a weakened or defective sphincter between the stomach and oesophagus leading to gastro-oesophageal reflux disease (GORD) with usually accompanying indigestion, heartburn and epigastric pain as well as dental erosion. Recurrent vomiting also has similar effects and this may be associated with irritable bowel syndrome or travel sickness, or it may be self-induced as occurs in the eating disorders of anorexia and bulimia nervosa. Extrinsic acids arise from dietary sources and whilst carbonated drinks and fruit juices are readily identified as being the cause, it should also be remembered that foods such as pickled vegetables, brown sauce and tomato ketchup do have erosive potential.

This erosion can affect any surface which comes into contact with the acid but it is more likely to occur on the occlusal and palatal surfaces of the maxillary teeth and to a lesser extent of the mandibular teeth.

Fig. 12.9 shows severe tooth surface loss as a result of excessive intake of carbonated drinks. The considerable erosion that has taken place is well demonstrated by the raised appearance of the amalgam restoration on the palatal surface of the maxillary right lateral incisor. The amalgam at the time of placement was flush with the enamel surface but now the latter is well below the original level. Fig. 12.10 shows erosion as a result of gastro-oesophageal reflux disease.

It is important that the condition is recognised at an early stage when the aetiological factors may be identified. Where it is dietary in origin, diet analysis and counselling will prevent further deterioration in the condition. Patients with gastro-oesophageal reflux disease or eating disorders should be referred initially to their medical practitioner. Where the amount of tooth loss has been mild and in the absence of tooth sensitivity, the condition may be left and the situation monitored at regular intervals to ensure that the wear has stopped. Where there has been a greater degree of surface loss, then restorative treatment by way of composite coatings, veneers or crowns may be required.

The method of erosion and abrasion (cervical lesions) treatment is as follows:

■ Access: this is not normally difficult unless the lesion is on the lingual surface of a molar tooth. The amount of cavity preparation depends on the cause of the lesion: abrasion and erosion lesions may only require the cutting of a bevel and cleaning of the cavity with a pumice and water paste, whereas carious cavities may require access with a high-speed round diamond bur and caries removal with an excavator or round stain-less steel slow-speed bur.

■ Material placement: resin composite is generally the material of choice for such restorations but amalgam may be placed in posterior teeth; in difficult, subgingival cavities glass ionomer-based materials may be used. Glass ionomers should be protected with either varnish or an unfilled resin for the first few days after placement to protect them from moisture contamination. The material may be shaped free-hand or with a matrix.

Clinical significance

It is important to recognize that excessive tooth wear is taking place and to diagnose the most likely cause. In many cases the causes may be multiple. Abrasion caused by tooth brushing may be reduced by improving brushing technique. A careful history and detailed notes on the position of the erosion are important in order to determine the precise cause. Dietary analysis and advice are essential for those suffering from erosion due to dietary causes.


In the case of excessive consumption of fluorine one can consider fluorosis to be un-carious lesion that occurs after teeth has been erupted. In endemic regions, fluorosis is considered to be an un-carious lesion that occur before teeth eruption, on the stage of dental follicle formation (for temporary dentition it is 4-5 m of intrauterine life, for permanent dentition it is 4-10 m of life).

Fig. Dental fluorosis. The abnormalities may vary from moderate (a) to severe (b). Enamel shows white spots,

brown discolorations, and surface irregularities indicating both enamel hypocalcification and hypomineralisation.


Over the last fifteen years it has been noted that an increasing number of infants and very young children have tended to swallow some of the tooth-paste used, and this is likely contributing to the increasing level of enamel fluorosis. Also, a pea-sized amount of toothpaste on the brush is more than adequate to clean young childrens teeth, but this amount (0.250.3 g) is often exceeded. Enamel fluorosis is a risk if too much fluoride toothpaste is used at too young an age and at too high a concentration.

Fluoride Supplements

Fluoride supplements are a risk factor for fluorosis in young children when used inappropriately and when not conforming to appropriate dosing schedules. Many studies have reported a clear association between supplement use by children aged less than 6 years and enamel fluorosis. Fluoride supplements can be prescribed for children at high risk of dental caries. When considering the prescription of fluoride supplements for children less than 6 years, dentists should weigh the risk for caries without fluoride supplements, the caries prevention offered by supplements and the potential for enamel fluorosis.

Risk Management for Enamel Fluorosis

A major risk factor in enamel fluorosis is inappropriate use of fluoride toothpaste at a young age. Use of fluoride toothpaste should continue due to the additive benefit from the combination of fluoridated water and toothpaste. The Forum on Fluoridation1 2002 recommends that parents should be advised to use a toothbrush and water to brush the teeth of children less than 2 years of age. Parents should consult professional advice with regard to the use of fluoride toothpaste when children are perceived to be at a high risk of dental decay. Children aged between 27 years of age should be supervised when brushing, using only a pea-sized amount of toothpaste and should also be encouraged to expectorate excess. The use of paediatric toothpastes with low concentrations of fluoride requires further research before they can be recommended. Having reviewed data from more recent studies were found that little decline in caries levels was observed between 0.7 and 1.2 ppm fluoride in water, while an increase in fluorosis was seen at this level. The authors suggested that a suitable trade-off between dental decay and fluorosis appears to occur at 0.7 ppm.


It is important to consider calcification and eruption dates of permanent teeth in order to identify when developing teeth are at most risk of enamel fluorosis (Tables 1 and 2). The occurrence of enamel fluorosis is strongly associated with cumulative fluoride ingestion during enamel development, but the severity of the condition depends on the dose, timing and duration of the fluoride intake. Permanent incisors begin calcifying at 34 months, and this is completed at 45 years (Table 2, Berkowitz et al. 1992).

The first year of life was the most critical period for developing fluorosis on aesthetically important maxillary central incisors. However, the greatest risk of fluorosis was associated with a four-month critical period starting at 22 months after birth. A more recent study showed that the first 3 years were the critical period for fluorosis on maxillary central incisors.

Table 1.


Table 2.


Acceptable measures of fluorine in water according to hygienic standards is 0,8-1,2(1,5) mg/l. Fluorosis is the term given to changes in the enamel which are associated with excess ingestion of fluoride. These vary from localised white opacities to more severe brownyellow mottling on the teeth. The precise effect depends on the dose of fluoride (from all sources), the duration for which it was taken and the age of the patient at the time of ingestion. Fluorosis when very severe (concentrations in the water supply greater than six parts per million) may result in extensive hypoplasia with brown staining.

Fluoride toxicity

Excessive ingestion of fluoride can result in fluorosis (mottling) which presents as opaque or white areas, lines or flecks in the enamel surface and can be cosmetically disfiguring when they occur on anterior teeth. Fluorosis can occur at different times and varies in severity. Fig. 11.2 shows very mild dental fluorosis (graded TF1) and Fig. 11.3 shows more severe fluorosis (graded TF3), classified by the York Review as being of aesthetic concern. The most important time is when ingestion of excessive fluoride occurs during enamel formation of the aesthetically important permanent upper anterior teeth at between 15 and 30 months of age, although this period can be extended from birth to 6 years.

More severe and cosmetically unacceptable cases of fluorosis are uncommon in the UK but these can result from the use of fluoride supplements in areas where the water is artificially fluoridated or where fluoride occurs naturally at the optimum level of 1 ppm.


It has been estimated that about 20% of all enamel defects in the UK are attributable to fluorosis but mainly of the mildest form (TF1). Most of the staining in mottled enamel is confined to the outer 50100 m, so if treatment is considered necessary this is usually by composite restorations or in severe cases (Fig.11.4) by crowning or veneers.

More severe toxicity can result in systemic disease such as osteoporosis and skeletal deformity (Table 11.3).



Trauma to the oral region occurs frequently and comprises 5% of all injuries for which people seek treatment. In preschool children the figure is as high as 18% of all injuries. Amongst all facial injuries, dental injuries are the most common of which crown fractures and luxations occur most frequently. An appropriate treatment plan after an injury is important for a good prognosis. Guidelines are useful for dentists and other health care professionals in delivering the best care possible in an efficient manner. The International Association of Dental Traumatology (IADT) has developed a consensus statement after a review of the dental literature and group discussions. The first set of guidelines was published by IADT in 2001. Experienced researchers and clinicians from various specialties were included in the group. In cases where the data did not appear conclusive, recommendations were based on the consensus opinion of the IADT board members. The guidelines represent the current best evidence, based on literature research and professional opinion. As is true for all guidelines, the health care provider must apply clinical judgment dictated by the conditions present in the given traumatic situation. The IADT does not guarantee favorable outcomes from following the Guidelines, but using the recommended procedures can maximize the chances of success. Because management of permanent and primary dentition differs significantly.


Uncomplicated crown fracture

Fracture involves enamel or dentin and enamel; the pulp is not exposed. Sensibility testing may be negative initially indicating transient pulpal damage; monitor pulpal response until a definitive pulpal diagnosis can be made.

Treatment: If tooth fragment is available, it can be bonded to the tooth. Urgent care option is to cover the exposed dentin with a material such as glass ionomer or a permanent restoration using a bonding agent and composite resin. Definitive treatment for the fractured crown may be restoration with accepted dental restorative materials


Fig. Uncomplicated crown fracture.

Fig. Uncomplicated crown fracture.


Complicated crown fracture

Fracture involves enamel and dentin and the pulp is exposed. Sensibility testing is usually not indicated initially since vitality of the pulp can be visualized. Follow up control visits after initial treatment includes sensibility testing to monitor pulpal status.

Treatment: In young patients with immature, still developing teeth, it is advantageous to preserve pulp vitality by pulp capping or partial pulpotomy. This treatment is also the choice in young patients with completely formed teeth. Calcium hydroxide and MTA (white) are suitable materials for such procedures.

In older patients, root canal treatment can be the treatment of choice, although pulp capping or partial pulpotomy may also be selected. If too much time elapses between accident and treatment and the pulp becomes necrotic, root canal treatment is indicated to preserve the tooth. In extensive crown fractures a decision must be made whether treatment other than extraction is feasible

Fig.1 Classification of tooth fractures.

Fig.2 Complicated crown fracture. Pulp is visible



Fig. 4. Complicated crown fracture


Crown-root fracture

Fracture involves enamel, dentin and root structure; the pulp may or may not be exposed. Additional findings may include loose, but still attached, segments of the tooth. Sensibility testing is usually positive.

Treatment: Treatment recommendations are the same as for complicated crown fractures (see above). In addition, attempts at stabilizing loose segments of the tooth by bonding may be advantageous, at least as a temporary measure, until a definitive treatment plan can be formulated


Fig. Crown and root fracture.

Root fracture

The coronal segment may be mobile and may be displaced. The tooth may be tender to percussion. Sensibility testing may give negative results initially, indicating transient or permanent pulpal damage; monitoring the status of the pulp is recommended. Transient crown discoloration (red or grey) may occur

Treatment: Reposition, if displaced, the coronal segment of the tooth as soon as possible. Check position radio graphically. Stabilize the tooth with a flexible splint for 4 weeks. If the root fracture is near the cervical area of the tooth, stabilization is beneficial for a longer period of time (up to 4 months).

It is advisable to monitor healing for at least 1 year to determine pulpal status. If pulp necrosis develops, root canal treatment of the coronal tooth segment to the fracture line is indicated to preserve the tooth.

Fig. 1 Root fracture.

Fig. 2 Horisontal fracture in upper left second premolar can be visible after root canal filling.

Fig.3 Root fracture in upper incisor


Fig. 4 Root and crown fracture.




Information was prepared by Levkiv M.O.